Two main experimental models of inflammation have been studied in the rat. One model is characterized by inflammation of fast onset, in which mast cells degranulate and fluid and plasma protein rapidly accumulate. The other is characterized by inflammation of slow onset, in which mast cells remain intact and fluid, plasma protein, and neutrophils progressively accumulate. The former inflammatory response is induced by antiserum to IgE (anti-IgE). H1 and H2 histamine receptor antagonists inhibit this reponse; inhibitors of arachidonate lipoxygenase, B.W. 775-C and nordihydroguairetic acid (NDGA), suppressed the response, although the effects were weak and variable; and indomethacin has no effect. The slow inflammatory response is induced by carrageenan and is inhibited by indomethacin and BW755-C. These two models of inflammation were further characterized by experiments with normal and mutant (mast cell-deficient) mice. The carrageenan-induced fluid and plasma protein accumulations were the same in both the normal and mutant mice, whereas the anti-IgE-induced fluid accumulation was higher in the normal than in the mutant mice. This observation is consistent with our previous findings that mast cells participate in the anti-IgE model but not in the carrageenan model.